Skip Navigation


European Heart Journal Advance Access originally published online on February 28, 2008
European Heart Journal 2008 29(7):843-845; doi:10.1093/eurheartj/ehn066
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
29/7/843-a    most recent
ehn066v1
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Related articles in EHJ
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Ellinor, P. T.
Right arrow Articles by Milan, D. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ellinor, P. T.
Right arrow Articles by Milan, D. J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Polymorphisms and atrial fibrillation: sorting the wheat from the chaff

Patrick T. Ellinor* and David J. Milan

Cardiovascular Research Center and Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston, MA 02114, USA

* Corresponding author. Tel: +1 617 726 4959, Fax: +1 617 726 2155. Email: pellinor@partners.org

This editorial refers to ‘The non-synonymous coding IKr-channel variant KCNH2-K897T is associated with atrial fibrillation: results from a systematic candidate gene-based analysis of KCNH2 (HERG)’{dagger} by M.F. Sinner et al., on page 907

Footnotes

The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.

The first 10% of the full text of this article appears below.

In the last 5 years, we have gained an increasing appreciation for the genetic contribution to atrial fibrillation (AF). While Mendelian families with AF have been reported, they have typically been considered rare. Studies from Framingham1 and Iceland2 have demonstrated a genetic basis for AF in the general population. Family members of those with AF have an odds ratios of ~1.8 for developing the arrhythmia. This risk is considerably greater for younger patients1,2 and those with lone AF.3

One approach to identify common genetic determinants of a disease in a population is . . . [Full Text of this Article]


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?

Related articles in EHJ:

The non-synonymous coding IKr-channel variant KCNH2-K897T is associated with atrial fibrillation: results from a systematic candidate gene-based analysis of KCNH2 (HERG)
Moritz F. Sinner, Arne Pfeufer, Mahmut Akyol, Britt-Maria Beckmann, Martin Hinterseer, Annette Wacker, Siegfried Perz, Wiebke Sauter, Thomas Illig, Michael Näbauer, Claus Schmitt, H.-Erich Wichmann, Albert Schömig, Gerhard Steinbeck, Thomas Meitinger, and Stefan Kääb
EHJ 2008 29: 907-914. [Abstract] [FREE Full Text]  



This article has been cited by other articles:


Home page
 J Clin PharmacolHome page
J.-P. Couderc, S. Kaab, M. Hinterseer, S. McNitt, X. Xia, A. Fossa, B. M. Beckmann, S. Polonsky, and W. Zareba
Baseline Values and Sotalol-Induced Changes of Ventricular Repolarization Duration, Heterogeneity, and Instability in Patients With a History of Drug-Induced Torsades de Pointes
J. Clin. Pharmacol., January 1, 2009; 49(1): 6 - 16.
[Abstract] [Full Text] [PDF]